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words, a higher renal perfusion pressure becomes necessary for the kidneys to
excrete the required amount of salt and water to precisely match the intake [ 1 ].
Under physiological circumstances, several neurohumoral mechanisms act in
concert to amplify the effectiveness of the pressure natriuresis mechanism by
directly increasing renal excretory capacity, before a measurable change in renal
perfusion pressure becomes manifest. The major modulatory mechanism that deter-
mines the effectiveness of the pressure natriuresis is the renin-angiotensin-
aldosterone system. Adequate suppression of the renin secretion by several-fold
increases in sodium intake facilitates commensurate increases of the renal excretory
capacity, so that blood pressure does not change chronically in the face of large
variations of sodium input. Conversely, if the activity of the renin-angiotensin-
aldosterone system cannot be adequately suppressed, proportional increases in
blood pressure are required to allow the kidneys to excrete the additional salt and
fluid and hypertension ensues. This situation is mimicked experimentally by con-
tinuous infusion of either angiotensin II or aldosterone in normal animals exposed
to high salt intake [ 2 ]. Primary reductions in renal excretory capacity cause chronic
increases in blood pressure owing to their effect of altering the pressure natriuresis
relationship. Decreased glomerular filtration rate or increased tubular reabsorption
would therefore initiate a compensatory increase in blood pressure that ultimately
serves to maintain fluid balance.
Influence of Renal Sympathetic Nerve Activity on Blood
Pressure Control by the Kidneys
The renal structures playing key roles in fluid homeostasis and control of blood
pressure described above receive adrenergic innervation. Renal vascular innervation
is distributed along the arterial segments in the cortex and outer medulla, including
interlobar, arcuate, interlobular arteries, and afferent and efferent arterioles.
Furthermore, adrenergic terminals to renal tubular epithelial cells are found along
all segments of the nephron, including the proximal tubule, thick ascending limb of
loop of Henle, distal convoluted tubule, and the collecting duct. Renin-secreting
granular cells of the juxtaglomerular apparatus also receive direct sympathetic
innervation [ 3 ].
In conjunction with the structural distribution, renal sympathetic nerve activity
(RSNA) has effects that control the function of the different mechanisms involved
in the modulation of the pressure natriuresis mechanism described above. Increased
RSNA causes direct increases in tubular sodium reabsorption and renal vasocon-
striction through activation of different subtypes of α-adrenergic receptors located
on tubular and vascular smooth muscle cells of the kidney [ 4 ]. These direct effects
of increased RSNA lead to a primary reduction of renal excretory capacity, com-
manding chronic alterations in the pressure natriuresis mechanism and ultimately
chronic increases in BP. Furthermore, activation of β-adrenergic receptors located
R. Iliescu and D.N. Şerban